The overall goal of this project is to develop and test a detailed neural and computational account of the brain mechanisms underlying speech motor sequence planning and their breakdown in stuttering. Persistent developmental stuttering affects more than three million people in the United States, and it can have profound adverse effects on social, psychological, and occupational well-being. Despite its world-wide prevalence and negative impact, stuttering has resisted explanation and effective treatment. This project investigates the hypothesis that stuttering is caused by a network-level neural disturbance rather than a disturbance in a single neural region, and the functional result of this disturbance is an impaired ability to use phonological and sensorimotor contextual cues to select and initiate motor programs for upcoming speech gestures. This hypothesis will be tested using a highly integrated combination of neuroimaging and modeling studies organized around the GODIVA neurocomputational model of speech motor sequencing. Study 1 involves the use perturbations of auditory feedback during speech in a functional MRI study of the brain mechanisms underlying speech timing adjustments based on sensorimotor context. Comparison of brain activities from AWS to fluent controls will identify the neural deficits underlying an impaired ability of adults who stutter (AWS) to adjust speech motor timing in response to auditory feedback. In Study 2, repetition suppression functional magnetic resonance imaging will be used to (i) refine our understanding of phonological representations underlying speech production in fluent adults, and (ii) identify anomalies in the phonological representations of AWS that may degrade the speech sequencing system's ability to recognize the proper context for generating the next speech gesture. Study 3 utilizes a large structural and functional neuroimaging dataset from children who stutter (CWS), AWS, and matched controls to disentangle primary neural deficits underlying stuttering from secondary deficits and compensatory mechanisms, and to identify potential sub-types of stuttering involving different neural anomalies. Study 4 is a modeling project that synthesizes the findings from Studies 1- 3 into a detailed neurocomputational account of speech motor sequencing in the normal brain and its breakdown in stuttering. Key benchmarks of success include the ability to replicate anomalous movement timing patterns and neural activity in AWS and CWS compared to fluent speakers. The resulting neurocomputational model of stuttering will constitute a significant milestone in the centuries-old effort to understand this perplexing disorder and will pave the way for designing and testing novel treatments that are aimed squarely at the primary neural deficits.